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Tlr and immune response: role of β- (1-4) - galactose terminal glycans in enhancement of immune response and protection against experimental visceral leishmaniasis

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Title Tlr and immune response: role of β- (1-4) - galactose terminal glycans in enhancement of immune response and protection against experimental visceral leishmaniasis
 
Creator Paul, Joydeep
 
Subject Cancer Biology and Inflammatory Disorder Division
 
Description Kala-azar orvisceral leishmaniasis (VL), caused by the protozoan parasite Leishmania donavani (LD), is gradually making inroads in different continents due to migration of
people and vectors. Production of proinflammatory cytokines by antigen presenting cells and microbicidal molecules (reactive oxygen species or ROS & nitric oxide or NO) by the
host cells are the key regulators for successful clearance of LD parasites. The control of LD infection requires generation of NO and activation of a strong Th1 response, mainly by up regulation IFN-gamma through interleukin-12 or IL-12, while disease progression is promoted by induction of interleukin-10 or IL-10. An increasing number of receptor families are being implicated in the recognition of
pathogen-associated molecular patterns (PAMP) by the cells of immune system. Among these, toll like receptors (TLRs) are key players, linking innate and adaptive arm of
immune system. Following infection, pathogen derived several exogenous components may bind with the toll receptors thereby initiating several signaling pathways and
ultimately leading to the production of pro or anti inflammatory cytokines and generation of inducible Nitric oxide synthase or iNOS. TLR ligands such as LPS, glycolipids, peptidoglycans, lipopeptides are shared by large group of micro organisms and allow recognition of wide range of microbial pathogens. Following receptor ligand association except TLR3, all other TLRs recruits cytoplasmic adaptor molecule myeloid differentiation
primary response protein88 (MyD88) in the Toll/IL-1 receptor domain of TLRs. Although,
unlike other TLRs, TLR4 engagement, cause activation through both the MyD88 dependent and independent pathways, thereby ultimately leading to activation of common signaling cascade involving extracellular signal-regulated kinase (ERK), P38 mitogenactivated protein kinase, stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB).The overall impact of this signaling pathway would be the initiation of a Th-1 type immune response.TLR mediated signalling becomes refractory in LD infection.
 
Date 2015-10-08
 
Type Thesis
NonPeerReviewed
 
Format application/pdf
 
Identifier http://www.eprints.iicb.res.in/2423/1/Joydeep_Paul_Thesis.pdf
Paul, Joydeep (2015) Tlr and immune response: role of β- (1-4) - galactose terminal glycans in enhancement of immune response and protection against experimental visceral leishmaniasis. PhD thesis, JU.
 
Relation http://www.eprints.iicb.res.in/2423/